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Raphael Mohr Robert Schierwagen Carolynne Schwarze-Zander Christoph Boesecke Jan-Christian Wasmuth Jonel Trebicka Jürgen Kurt Rockstroh 《Medicine》2015,94(50)
Liver-related death in human immunodeficiency virus (HIV)-infected individuals is about 10 times higher compared with the general population, and the prevalence of significant liver fibrosis in those with HIV approaches 15%. The present study aimed to assess risk factors for development of hepatic fibrosis in HIV patients receiving a modern combination anti-retroviral therapy (cART).This cross-sectional prospective study included 432 HIV patients, of which 68 (16%) patients were anti-hepatitis C virus (HCV) positive and 23 (5%) were HBsAg positive.Health trajectory including clinical characteristics and liver fibrosis stage assessed by transient elastography were collected at inclusion. Liver stiffness values >7.1 kPa were considered as significant fibrosis, while values >12.5 kPa were defined as severe fibrosis. Logistic regression and Cox regression uni- and multivariate analyses were performed to identify independent factors associated with liver fibrosis.Significant liver fibrosis was detected in 10% of HIV mono-infected, in 37% of HCV co-infected patients, and in 18% of hepatitis B virus co-infected patients. The presence of diabetes mellitus (odds ratio [OR] = 4.6) and FIB4 score (OR = 2.4) were independently associated with presence of significant fibrosis in the whole cohort. Similarly, diabetes mellitus (OR = 5.4), adiposity (OR = 4.6), and the FIB4 score (OR = 3.3) were independently associated with significant fibrosis in HIV mono-infected patients. Importantly, cumulative cART duration protected, whereas persistent HIV viral replication promoted the development of significant liver fibrosis along the duration of HIV infection.Our findings strongly indicate that besides known risk factors like metabolic disorders, HIV may also have a direct effect on fibrogenesis. Successful cART leading to complete suppression of HIV replication might protect from development of liver fibrosis. 相似文献
144.
C. Banella M. Ginevrino G. Catalano E. Fabiani G. Falconi M. Divona P. Curzi P. Panetta M.T. Voso N.I. Noguera 《Hematology/oncology and stem cell therapy》2021,14(2):163-168
FGFR–TACC, found in different tumor types, is characterized by the fusion of a member of fibroblast grown factor receptor (FGFR) tyrosine kinase (TK) family to a member of the transforming acidic coiled-coil (TACC) proteins. Because chromosome numerical alterations, hallmarks of FGFR–TACC fusions are present in many hematological disorders and there are no data on the prevalence, we studied a series of patients with acute myeloid leukemia and myelodysplastic syndrome who presented numerical alterations using cytogenetic traditional analysis. None of the analyzed samples showed FGFR3–TACC3 gene fusion, so screening for this mutation at diagnosis is not recommended. 相似文献
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Miguel A. Sanz Pau Montesinos Haesook T. Kim Guillermo J. Ruiz-Argüelles María S. Undurraga María R. Uriarte Lem Martínez Rafael H. Jacomo Homero Gutiérrez-Aguirre Raul A. M. Melo Rosane Bittencourt Ricardo Pasquini Katia Pagnano Evandro M. Fagundes Edo Vellenga Alexandra Holowiecka Ana J. González-Huerta Pascual Fernández Javier De la Serna Salut Brunet Elena De Lisa José González-Campos José M. Ribera Isabel Krsnik Arnold Ganser Nancy Berliner Raul C. Ribeiro Francesco Lo-Coco Bob L?wenberg Eduardo M. Rego 《Annals of hematology》2015,94(8):1347-1356